Botulism

Botulism is an acute neurologic disorder that causes potentially life-threatening neuroparalysis due to a neurotoxin produced by Clostridium botulinum. The toxin binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions. Toxin binding blocks acetylcholine release, resulting in weakness, flaccid paralysis, and, often, respiratory arrest. Cure occurs following sprouting of new nerve terminals.

The 3 main clinical presentations of botulism include infant botulism or intestinal botulism, foodborne botulism, and wound botulism.  Iatrogenic botulism may also occurr via cosmetic or therapeutic injection of any commercially made botulinum toxin (e.g. Botox, Dysport, Xeomin, Myobloc).  Additionally, because of the potency of the toxin and ease of aerosolization, the possibility of inhalational botulism as a bioterrorism agent or biological weapon is of great concern[9] .  For more information, see CBRNE – Botulism.

Infant botulism is caused by ingested C botulinum spores that germinate in the intestine and produce toxin. These spores typically come from the environment.[10]  Natural honey and corn syrup have been theorized as sources, however, most infants with botulism have not been exposed to honey. Most infants fully recover with supportive treatment; the attributed infant mortality rate is less than 1%.[11]  Improperly canned or home-prepared foods are common sources of the toxin that can result in foodborne botulism. Wound botulism results from contamination of a wound with toxin-producing C botulinum. Foodborne botulism and wound botulism occur predominantly in adults and are the focus of this article.

C botulinum is an anaerobic gram-positive rod that survives in soil and marine sediment by forming spores.[1]  Under anaerobic conditions that permit germination, it synthesizes and releases a potent exotoxin. On a molecular weight basis, botulinum toxins are the most potent toxins known.

Seven antigenically distinct C botulinum toxins are known, including A, B, C, D, E, F, and G[4] . Each strain of C botulinum can produce only a single toxin type. Types A, B, E, and, rarely, F cause human disease.[1]  Toxins A and B are the most potent, and the consumption of small amounts of food contaminated with these types has resulted in full-blown disease. During the last 20 years, toxin A has been the most common cause of foodborne outbreaks; toxins B and E follow in frequency.

The mechanism of action involves toxin-mediated blockade of neuromuscular transmission in cholinergic nerve fibers. This is accomplished by inhibiting acetylcholine release at the presynaptic clefts of the myoneural junctions. Toxins are absorbed from the stomach and small intestine, where they are not denatured by digestive enzymes. Subsequently, they are hematogenously disseminated to peripheral cholinergic nerve terminals (neuromuscular junctions, postganglionic parasympathetic nerve terminals, peripheral ganglia). The toxin is endocytosed by the neuron and is then allowed to cleave proteins essential for neurotransmitter release. The toxin does not cross the blood-brain-barrier, likely secondary to its large size, however, it may be transported to the central nervous system axonally.[12]

Because the motor end plate responds to acetylcholine, botulinum toxin ingestion results in hypotonia that manifests as descending symmetric flaccid paralysis and is usually associated with gastrointestinal symptoms of nausea, vomiting, and diarrhea. Cranial nerves are affected early in the disease course. Later complications include paralytic ileus, severe constipation, and urinary retention.

Humans commonly ingest C botulinum spores, but germination does not typically occur in the adult intestine since special conditions are required (ie, anaerobic environment, low acidity, specific amino acid, salt and sugar concentrations, and temperatures 37oF-99oF).[1, 11]

Wound botulism results when wounds are contaminated with C botulinum spores. Wound botulism has developed following traumatic injury that involved soil contamination, among injection drug users (particularly those who use black-tar heroin and rarely after cesarean delivery.[13, 14] The wound may appear deceptively benign. Traumatized and devitalized tissue provides an anaerobic medium for the spores to germinate into vegetative organisms and to produce neurotoxin, which then disseminates hematogenously. Symptoms develop after an incubation period of 4-13 days, with a median 6.5 day.[15]  The clinical symptoms of wound botulism are similar to those of foodborne botulism except that gastrointestinal symptoms (including nausea, vomiting, diarrhea) are uncommon.

In the United States over 100 cases of botulism are reported annually to the Centers for Disease Control and Prevention (CDC). Infant botulism with mean age of 13 weeks accounts for 60-70% of all botulism cases.[16, 10]

The incidences of foodborne and wound botulism are similar as of 2017.[17, 18]  Disease due to Toxin A is found predominantly west of the Mississippi River in wound botulism. Toxin B is found most commonly in the eastern United States associated with infant botulism. Toxin E is found in northern latitudes, such as the Pacific Northwest, the Great Lakes region, and Alaska. The frequency of botulism in native Alaskans is among the highest in the world, uniquely implicating fermented beaver tail as the source of foodborne botulism in recent history[19] . Toxin E outbreaks are also frequently associated with fish products.[20]

Mortality rates vary based on the age of the patient and the type of botulism and have significantly declined over the last century due to improvements in supportive care.  The modern mortality for foodborne botulism is 5% or less.[1, 21]  Wound botulism carries a mortality rate of roughly 10%.[22]  The risk of death due to infant botulism is usually less than 1%.[10]

The recovery period from botulism flaccid paralysis takes weeks to months.[4]  Death that occurs early in the course of disease is usually secondary to acute respiratory failure, whereas death later in the course of illness is typically secondary to complications associated with prolonged intensive care (eg, venous thromboembolism or hospital-acquired infection). Some patients demonstrate residual weakness or autonomic dysfunction for 1 year after the onset of the illness. However, most patients achieve full neurologic recovery. Permanent deficits may occur in those who sustain significant hypoxic insults.

Sex

Wound botulism is more common in females.[16]  Foodborne botulism has no sexual predilection.

Age

Foodborne botulism and wound botulism predominately occur in adults. The mean age of infant botulism is 3 months[10] .

Following the onset of symptoms, botulism quickly progresses over several days. The magnitude of the neuromuscular impairment can advance hourly. Persons who survive this phase eventually stabilize and then recover over a period of days to months. The mechanism of recovery is not fully understood but requires the generation of new presynaptic axons and the formation of new synapses, as the original synapses are permanently affected. As with tetanus, recovery from botulism does not confer long-term immunity. Rare reports have described a second episode in the same patient.

Foodborne botulism

Foodborne botulism should be suspected in patients who present with an acute gastrointestinal illness associated with neurologic symptoms. Symptoms a median of 1 day following consumption of contaminated food produc.[23]  The severity of the illness varies from mild to severe, and death occurs at a median of 3 days after hospitalization. The modern case fatality ratio is 9%.

Wound botulism

Patients with wound botulism typically have a history of traumatic injury with wounds that are contaminated with soil.[24]

Since 1994, the number of patients with wound botulism who have a history of chronic intravenous drug abuse has increased dramatically. In most cases, black-tar heroin has been the implicated vehicle. A study by Yuan et al followed 17 heroin users who had recurrent botulism after using black-tar heroin.[13]  Physicians need to be alert to recognize botulism, especially in patients who use black-tar heroin or in those with a history of injection drug–associated botulism.

Rare cases of wound botulism after cesarean delivery have been documented.[14]

Aside from a longer incubation period, wound botulism is similar to foodborne botulism. The incubation period of wound botulism ranges from 4-13 days, with a median 6.5 days.[15]  Unlike foodborne botulism, gastrointestinal symptoms (including nausea, vomiting, diarrhea) are uncommon in wound botulism. Patients may be febrile, but this is more likely due to the wound infection rather than the wound botulism. In many cases, the wound appears benign.

Adult intestinal toxemia

Adult intestinal toxemia results from enteric colonization with C botulinum that progresses to toxin production. The pathophysiology of the changes in the gastrointestinal flora that facilitate colonization is unclear.[25]

Iatrogenic botulism due to accidental overdose of botulinum toxin (Botox or Dysport)

Cases of botulism due to Botox overdosage have been reported. Symptoms vary and can include dysphagia, ptosis, and diplopia, as well as more severe presentations of systemic weakness or muscle paralysis.[26]

Almost all patients with foodborne or intestinal exposure are afebrile and the majority of patients will display descending paralysis with cranial nerve palsies early in the disease process.  A collection of anticholinergic toxicity symptoms will present such as nausea, vomiting, dysphagia, diplopia, dilated/fixed pupils, and dry mouth.[9]  Mydriasis is seen in 50% of cases.

Generally, botulism progresses as follows:

• Preceding or following the onset of paralysis are nonspecific findings such as nausea, vomiting, abdominal pain, malaise, dizziness, dry mouth, dry throat, and, occasionally, sore throat. Except for nerves I and II, the cranial nerves are affected first.

• Cranial nerve paralysis manifests as blurred vision, diplopia, ptosis, extraocular muscle weakness or paresis, fixed/dilated pupils, dysarthria, dysphagia, and/or suppressed gag reflex. Additional neurologic manifestations include symmetric descending paralysis or weakness of motor and autonomic nerves.

• Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure. Progressive muscle weakness occurs and often involves the muscles of the head and neck, as well as intercostal diaphragmatic muscles and those of the extremities.

The autonomic nervous system is also involved. Manifestations of this include the following:

• Paralytic ileus advancing to severe constipation

• Gastric dilatation

• Bladder distention advancing to urinary retention

• Orthostatic hypotension

• Reduced salivation

• Reduced lacrimation

Other neurologic findings include the following:

• Changes in deep tendon reflexes, which may be either intact or diminished

• Incoordination due to muscle weakness

• Absence of pathologic reflexes and normal findings on sensory and gait examinations

• Normal results on mental status examination

Wound botulism

Causes of wound botulism have been associated with traumatic injury involving contamination with soil, chronic abuse of intravenous drugs (eg, black-tar heroin), and rarely cesarean delivery. Wound botulism illness can occur even after antibiotics are administered to prevent wound infection.  Wound botulism from black-tar heroin use has primarily occurred in California.[16]

Foodborne botulism

Of the roughly 110 cases of botulism that occur in the US annually, foodborne exposure accounts for ~25% of cases.[16]   It results from the ingestion of preformed neurotoxins; A, B, and E are the most common.  California, Washington, Colorado, Oregon and Alaska, have accounted for >50% of reported foodborne outbreaks in the US since 1950.

High-risk foods include home-canned or home-processed low-acid fruits, vegetables, fish and fish products (neurotoxin serotype E).[20]

Commercially processed foods and improperly handled fresh foods are occasionally associated with botulism outbreaks.  The type of food responsible for approximately 28% of outbreaks remains unknown.

High clinical suspcicion and clinical diagnosis with immediate antitoxin administration is the cornerstone of management, as laboratory tests are not helpful in the routine diagnosis of botulism.[6]  

A clinical criteria tool for early diagnosis has been developed for outbreak settings.[27]  

When botulism is suspected, consult public health officials immediately, request antitoxin, and if transferring to a higher level of care consider administering antitoxin before transfer.[28]  Full neurologic exam, brain imaging, lumbar puncture, electromyography, nerve conduction studies, and monitoring for anaphylaxis after antitoxin administration should be performed as applicable.

WBC counts and erythrocyte sedimentation rates are usually normal.[29]  Cerebrospinal fluid is also normal, except for occasional mild elevations in protein concentration.

Laboratory confirmation of botulism requires either botulinum neurotoxin isolation or growth of a botulinum neurotoxin-producing ​Clostridium species (ie, C botulinum, C baratii, or C butyricum) in a stool, gastric aspirate, food, or wound culture. 

Botulinum neurotoxin isolation requires intraperitoneal injection of the patient' serum, fluid extract of food or feces, etc. into pairs of mice with and without monovalent antitoxin followed by observation for development of clinical botulism.[6, 30]  This test was standardized in the 1970s and has limited sensitivity depending on the mode of toxin exposure. These assays are limited to specific state public health and CDC laboratories, where other assays may also be used to determine neurotoxin serotype. Patient samples must be collected prior to administration of antitoxin, but antitoxin administration must not be delayed in order to obtain samples (serum 5-15 mL, stool 10-20 g, gastric aspirate 5-10 mL, suspected food source 10-20 g or mL).[1]   

To send a specimen to the CDC for testing[1] :

• Call CDC consultant to discuss submission of specimens through local or state health department or state public health laboratory
• Maintain the specimen at 36 ^oF-46 ^oF and ship with cold packs
• Label package as required for Category B substances
• Include completed CDC 50.34 with selected test order CDC-10132, Botulism Laboratory Confirmation and include phone and fax numbers for the state health department and hospital
• Send package to: STAT (Attn: Botulism Lab, Unit 26) Centers for Disease Control and Prevention1600 Clifton Rd NE, Atlanta, GA 30329
• Provde a tracking number to the CDC National Botulism Laboratory 

C botulinum may be grown on selective media from samples of stool or foods. Note that the specimens for toxin analysis should be refrigerated (not frozen), but culture samples of C botulinum should not be refrigerated.  Final results from culture for Clostridium species may take 2-3 weeks.

Because intestinal carriage is rare (and adult intestines typically do not allow for germination), identifying the organism or its toxin in vomitus, gastric fluid, or stool strongly suggests the diagnosis.[4]  Isolation of the organism from food without toxin is insufficient grounds for the diagnosis. Only experienced personnel who have been immunized with botulinum toxoid should handle the specimens. Because the toxin may enter the blood stream through the eye or via small breaks in the skin, precaution is warranted.

Wound cultures that grow C botulinum suggest of wound botulism.

Imaging studies are generally not useful in the diagnosis of botuli.[31]

The only potential role for imaging studies (eg, CT scan, MRI) would be to rule out CNS pathology, such as intracranial mass lesions, cerebrovascular disease of the brainstem, or basilar artery stroke, in patients in whom the presentation is atypical or vague.

Results from nerve conduction studies are normal, and electromyography (EMG) reveals reduced amplitude of compound muscle action potentials.[7, 8]

EMG may be useful in establishing a diagnosis of botulism, but the findings can be nonspecific and nondiagnostic, even in severe cases. Characteristic findings in patients with botulism include brief low-voltage compound motor-units, small M-wave amplitudes, and overly abundant action potentials. An incremental increase in M-wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction. Single-fiber EMG may be a more useful and sensitive method for the rapid diagnosis of botulism intoxication, particularly in the absence of signs of general muscular weakness.

The results of the edrophonium chloride, or Tensilon, test for myasthenia gravis may be falsely positive in patients with botulism.[32]  If positive, it is typically much less dramatically positive than in patients with myasthenia gravis.

Antitoxin

On March 22, 2013, the FDA approved the first botulism antitoxin that can neutralize all 7 known botulinum nerve toxin serotypes.[33]  The heptavalent antitoxin is derived from horse plasma and is the only drug available for treating botulism in patients older than 1 year, including adults. It is also the only available drug for treating infant botulism that is not caused by nerve toxin type A or B; otherwise, human-origin anti-A, anti-B botulinum antitoxin (BabyBIG) should be obtained from the California Infant Botulism Treatment and Prevention Program at +1 510-231-7600 (do not use equine antitoxin for infants).[34]

Older literature on anti-ABE trivalent antitoxin does suggest that it reduces mortality (Odds Ratio [OR], 0.22; CI 0.17-0.29) most significantly against botulism types E(OR, 0.13; CI, 0.06-0.30) and A (OR, 0.57; C, 0.39-0.84).[1, 35]  

BAT® [Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) - (Equine)].[1, 36]

See the list below:

• Ideally should be administered within 24 hours of symptom onset as the antitoxin cannot reverse existing paralysis, only toxin circulating in the blood.  The greatest benefit is seen among those who receive it within 2 days of illness onset.  However, regardless of time after disease onset, patients should still receive antitoxin to protect unaffected synapes from persistent circulating toxin, which is known to persist for weeks in the blood. ^[37]
• Consult local or state health department immediately and the 24-hour CDC botulism service to request antitoxin (+1 404-639-2206 or +1 770-488-7100) 
• The standard adult dose for patients >55 kg is one vial (10-22 mL per vial) diluted 1:10 in normal saline by slow intravenous infusion (0.5-2 mL/min)
• Adverse effect frequencies (all recently observed adverse effects are nonserious) ^[38]

  See the list of potential adverse effects: 

• 3% Fever
• 2% Rash
• 1% Chills
• 1% Agitation/ anxiety
• 1% Edema
• 1% Elevated blood pressure
• 1% Nausea
• < 1% Mild serum sickness (e.g. fever, urticarial or maculopapular rash, myalgia, arthralgia, and lymphadenopathy) may occur 10-21 days after administration
• 5% Other: bronchospasm, chest pressure, diaphoresis, erythema, increased respiratory rate, “jitteriness,” leukocytosis, mild hypotension, tachycardia, urinary retention, and vomiting
• As the half-lives of the antittoxin range from 7.5-34 hours, it is plausible that exposure to a high concentration of toxin may require a second dose of BAT.  If disease progression worsens after the first dose should have taken effect and suspicion remains high (ie, known outbreak setting or exposure history), a second dose can be provided within 2 weeks (to avoid devloping hypersensitivity reaction to the antitoxin).  ^[1]  However, toxin exposure of this magnitude would be a rare occurence and other diagnoses should be considered in this case. 
• Pregnant women with suspected botulism should be treated with BAT just as nonpregnant patients 

See the BAT® package insert here.

Antibiotics

Antibiotics have no role in the treatment of foodborne or intestinal botulism. Wound botulism may require surgical debridement and antibiotic therapy because of wound infection (Clostridium may be targeted with penicillin or metronidazole). Of note, aminoglycosides should be avoided in patietns with botulism as they may aggravate disease through inhibition of presynaptic calcium uptake, which is required for acetylcholine release.[39]

Supportive Care

It is important to remember that patients with flaccid paralysis from botulism do not have sensory or cognitive impairment from the toxin.

Rigorous and supportive care is essential in patients with botulism.

Meticulous airway management is paramount, as respiratory failure is the most important threat to survival in patients with botulism.

Patients with symptoms of botulism or known exposure should be hospitalized and closely observed.

Spirometry, pulse oximetry, vital capacity, and arterial blood gases should be evaluated sequentially.

Respiratory failure can occur with unexpected rapidity.

Extrapolating from Guillain-Barré syndrome, intubation and mechanical ventilation should be strongly considered when the vital capacity is less than 20 mL/kg, especially when paralysis is progressing rapidly and hypoxemia with hypercarbia is present.[40]

Many patients require intubation and ventilatory support for a few days to months.

Tracheostomy may prove necessary to manage secretions.

Patients with bowel sounds are administered cathartics and enemas to remove unabsorbed botulinum toxin from the intestine.

Magnesium salts, citrate, and sulfate should not be administered because magnesium can potentiate the toxin-induced neuromuscular blockade.

Stress ulcer prophylaxis is also a standard component of intensive care management.

If an ileus is present, nasogastric suction and intravenous hyperalimentation are very helpful supportive measures. If no ileus is present, tube feeding can be used for nutritional supplementation.

A Foley catheter is often used to treat bladder incontinence. This must be monitored conscientiously and changed regularly.

Measures to reduce the risk of nosocomial infections include the following:

• Close observation for hospital-acquired infections, especially pneumonia (particularly aspiration pneumonia), is necessary, as is precaution to prevent aspiration. Aggressive pulmonary toilet with clearance of secretions, ventilatory support, and incentive spirometry are typically used.

• Close observation for urinary tract infection is essential. Foley catheters should be changed on a regular basis.

• Meticulous skin care is required to prevent decubital ulcers and skin breakdown.

• Careful attention to peripheral and central intravenous catheters with regular site rotation to reduce the risks of thrombophlebitis, cellulitis, and line infections should be part of the supportive care.

• Deep venous thrombosis (DVT) prophylaxis is also a standard component of intensive care management.

Wound botulism requires incision and thorough debridement of the infected wound, antitoxin therapy, and antibiotics should be provided as clinically indicated.  

A nutritionist should be consulted for hyperalimentation and tube-feeding recommendations and monitoring.

Physical and occupational therapists are needed to work on range-of-motion exercises and assisted ambulation, as tolerated.

A psychiatrist and/or a psychologist is recommended for counseling, as needed; patients with prolonged hospitalization, slow recovery, and complications from the disease or from extended hospitalization are at increased risk for depression.

Pastoral care is recommended, as needed.

Physical medicine and rehabilitation specialists may be helpful in coordinating long-term rehabilitation planning once sustained recovery has begun.

Nasogastric suction and intravenous hyperalimentation are important when an ileus is present. If no ileus is present or when the ileus resolves, tube feeding can be used for nutritional supplementation.

Oral intake should be reinstituted gradually under the following conditions:

• Respiratory status is stable without mechanical ventilation.

• Swallowing safety has been assessed and confirmed with a swallowing study, as appropriate.

• Ileus has resolved.

Bedrest is initially required.

Increase activity as tolerated.

CDC - Clinical Guidelines for Diagnosis and Treatment of Botulism, 2021

Antibiotics are useful in wound botulism, but they have no role in foodborne botulism.

Class Summary

When botulism develops following a wound infection, antibiotic therapy and meticulous debridement of the wound are essential.

Penicillin G (Pfizerpen)

Preferred drug of choice for wound botulism. Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Metronidazole (Flagyl, Flagyl ER, Flagyl IV RTU)

Class Summary

These agents are essential in the treatment of foodborne botulism and wound botulism. Heptavalent antitoxin (toxins A through G) is available at the Centers for Disease Control and Prevention (CDC). The CDC phone number is (770) 488-7100.  Because of the risk of adverse reactions and lack of human clinical data, prophylactic antitoxin is not recommended in patients who are exposed to botulism toxin but who have no symptoms - however, it may be considered after a known high risk exposure as an extraordinary measure[9] .

Botulinum antitoxin, heptavalent (HBAT)

Antitoxin indicated for naturally occurring noninfant botulism. Equine-derived antitoxin that elicits passive antibody (ie, immediate immunity) against Clostridium botulinum toxins A, B, C, D, E, F, and G.

Each 20-mL vial contains equine-derived antibody to the 7 known botulinum toxin types (A through G) with the following nominal potency values: 7500 U anti-A, 5500 U anti-B, 5000 U anti-C, 1000 U anti-D, 8500 U anti-E, 5000 U anti-F, and 1000 U anti-G.

Replaces licensed bivalent botulinum antitoxin AB (BAT-AB) and investigational monovalent botulinum antitoxin E (BAT-E). To obtain, contact CDC Emergency Operations Center; telephone: (770) 488-7100. Product to be stored in Strategic National Stockpile for emergency preparedness and responses.

The most significant improvements in ventilatory and upper airway muscle strength occur over the first few months, and, in some patients, recovery may not be complete for as long as a year.  Residual symptoms such as fatigue and shortness of breath may linger for years.[41]  Close follow-up is crucial.

Follow-up with other consultants, such as physical medicine and rehabilitation specialists, physical and occupational therapists, nutritionists, and psychiatrists, should be obtained as needed.

Neurologic Monitoring

Serial neurologic examination focusing on bulbar nerves and respiratory status should be performed with frequency of examination tailored to rapiditiy of disease progression.[1]

Respiratory Monitoring

Apart from early receipt of BAT (within 12 hours of presentation), there are no known specific signs or symptoms that suggest which patients with botulism will develop respiratory failure, therefore, respiratory monitoring can be extrapolated from management of other neuromuscular syndromes such as Guillian-Barré or Myasthenia Gravis.[42]  

Patients with rising end-tidal CO2, forced vital capacity < 20 mL/kg, maximum negative inspiratory force < 30 cm H2O, and maximum expiratory pressure < 40 cm H2O may require intubation.[40]  

Autonomic Nervous System Monitoring

Dysautonomia due to unopposed sympathetic nervous system stimulation is a hallmark of poisonin with toxin type B and may require cardiac and blood pressure monitoring.[1, 43]

Recovery of ventilatory and upper airway muscle strength in patients who develop respiratory failure is most significant over the first few months. The time for recovery typically ranges from 30-100 days as recovery necessitates axonal regeneration. Artificial respiratory support may be required for months in severe cases.

Transfer is indicated if the patient's condition continues to deteriorate or if the initial hospital is unable to manage the complexities involved.

Prompt notification of public health authorities regarding a suspected case of botulism may prevent further consumption of a contaminated home-canned or commercial food product.

Foodborne botulism is best prevented by strict adherence to recommended home-canning techniques.[44, 45]  High-temperature pressure cooking is essential to ensure spore elimination from low-acid fruits and vegetables. Although boiling for 10 minutes kills bacteria and destroys the heat labile botulism toxin, the spores are resistant to heat and can survive boiling for 3-5 hours. Food contaminated by botulism toxins usually has a putrefactive odor; however, contaminated food may also look and taste normal. Hence, terminal heating of toxin-containing food can prevent illness and is an important preventive measure.

Wound botulism is best prevented by prompt thorough debridement of contaminated wound.[1]  

Nosocomial infections

Hospital-acquired pneumonia, especially aspiration pneumonia, can occur.[4]  Atelectasis and poor secretion clearance also increase the risk of hospital-acquired pneumonia.[46]

Urinary tract infection can occur from in-dwelling Foley catheters.[47]

Skin breakdown and pressure ulcer formation can occur with prolonged mobility impairment.  Multiple combined interventions can be effective in their prevention.[48]

Thrombophlebitis, cellulitis, and line infections can occur. These patients often have peripheral and central intravenous catheters for prolonged periods.[49]

Fungal infections can occur; the predisposing factors include prolonged hospitalization, parenteral nutrition, and central venous catheters.[50]

DVT prophylaxis is essential to reduce the risk of these potential complications. DVT and pulmonary embolism (PE) are potential complications because patients can be bedridden for weeks to months.

Stress ulcers can occur and are common in the intensive care unit setting, espcecially in critically ill patients. Stress ulcer prophylaxis with either proton-pump inhibitor or H2 antagonist should be considered to reduce the risk of this potential complication.[51]

Other potential complications

Other potential complications include the following:

• Hypoxic tissue damage can lead to permanent neurologic deficits.

• Death

Botulism due to type A toxin is generally more severe than that caused by type B or E.

Mortality rates vary based on the age of the patient and the type of botulism and have significantly declined over the last century due to improvements in supportive care.  The modern mortality for foodborne botulism is 5% or less.[1, 21]  Wound botulism carries a mortality rate of roughly 10%.[22]  The risk of death due to infant botulism is usually less than 1%.[10]

The recovery period from botulism flaccid paralysis takes weeks to months.[4]  Death that occurs early in the course of disease is usually secondary to acute respiratory failure, whereas death later in the course of illness is typically secondary to complications associated with prolonged intensive care (eg, venous thromboembolism or hospital-acquired infection). Some patients demonstrate residual weakness or autonomic dysfunction for 1 year after the onset of the illness. However, most patients achieve full neurologic recovery. Permanent deficits may occur in those who sustain significant hypoxic insults.

Mortality is due to the following:

• Delayed diagnosis and respiratory failure

• Hospital complications such as nosocomial infections (usually pneumonia)

When preserving food at home, kill C botulinum spores by pressure cooking at 250°F (120°C) for 30 minutes.[20, 44]  The toxin can be destroyed by boiling for 10 minutes or cooking at 175°F (80°C) for 30 minutes. Do not eat or taste food from bulging cans. Discard food that smells bad.

Cessation of intravenous drug use prevents wound botulism due to this vehicle.